Gulati, Abhilasha and Mahadevan, Subramony (2000) Mechanism of catabolite repression in the bgl operon of Escherichia coli: involvement of the anti-terminator BglG, CRP - cAMP and $EIIA^G^L^c$ in mediating glucose effect downstream of transcription initiation. In: Genes to Cells, 5 (4). pp. 239-250.
Background: Expression of the bgl operon of Escherichia coli, involved in the regulated uptake and utilization of aromatic \beta-glucosides, is extremely sensitive to the presence of glucose in the growth medium. We have analysed the mechanism by which glucose exerts its inhibitory effect on bgl expression. Results: Our studies show that initiation of transcription from the bgl promoter is only marginally sensitive to glucose. Instead, glucose exerts a more significant inhibition on the elongation of transcription beyond the rho-independent terminator present within the leader sequence. Transcriptional analyses using plasmids that carry mutations in bglG or within the terminator, suggest that the target for glucose-mediated repression is the anti-terminator protein, BglG. Introduction of multiple copies of bglG or the presence of mutations that inhibit its phosphorylation by Enzyme $II^B^g^l (BglF)$, result in loss of glucose repression. Studies using crp, cya and crr strains show that both CRP-cAMP and the Enzyme $IIA^G^l^c (EIIA^G^l^c)$ are involved in the regulation. Although transcription initiation is normal in a crp, cya double mutant, no detectable transcription is seen downstream of the terminator, which is restored by a mutation within the terminator. Transcription past the terminator is also partly restored by the addition of exogenous cAMP to glucose-grown cultures of a crp(+) strain. Glucose repression is lost in the crr mutant strain. Conclusions: The results summarized above indicate that glucose repression in the bgl operon is mediated at the level of transcription anti-termination, and glucose affects the activity of BglG by altering its phosphorylation by BglF. The CRP-cAMP complex is also involved in this regulation. The results using the crr mutant suggest a negative role for $EIIA^G^l^c$ in the catabolite repression of the bgl genes.
|Item Type:||Journal Article|
|Additional Information:||Copyright for this article belongs to Blackwell Science Ltd.|
|Department/Centre:||Division of Biological Sciences > Molecular Reproduction, Development & Genetics (formed by the merger of DBGL and CRBME)|
|Date Deposited:||24 May 2005|
|Last Modified:||19 Sep 2010 04:15|
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